Group B/2 resistant Ambrosia artemisiifolia from United States, Wisconsin

International Survey of Herbicide-Resistant Weeds

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Monday, July 22, 2019

GROUP B/2 RESISTANT COMMON RAGWEED
(Ambrosia artemisiifolia)

ALS inhibitors (B/2)

United States, Wisconsin

INTRODUCTION		COMMON RAGWEED
Common Ragweed (Ambrosia artemisiifolia) is a dicot weed in the Asteraceae family. In Wisconsin this weed first evolved resistance to Group B/2 herbicides in 2013 and infests Soybean. Group B/2 herbicides are known as ALS inhibitors (Inhibition of acetolactate synthase ALS (acetohydroxyacid synthase AHAS)). Research has shown that these particular biotypes are resistant to cloransulam-methyl and they may be cross-resistant to other Group B/2 herbicides. The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

QUIK STATS (last updated Mar 25, 2015 )
Common Name	Common Ragweed
Species	Ambrosia artemisiifolia
Group	ALS inhibitors (B/2)
Herbicides	cloransulam-methyl
Location	United States, Wisconsin
Year	2013
Situation(s)	Soybean
Contributors - (Alphabetically)	Thomas Butts, Vince Davis (moved), and David Stoltenberg
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NOTES ABOUT THIS BIOTYPE

GENERAL

David Stoltenberg

A fact sheet documenting the ALS inhibitor resistant common ragweed from Wisconsin is available.

Click Here for Fact Sheet

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ACADEMIC ASPECTS

Confirmation Tests

Field, and Greenhouse trials comparing a known susceptible Common Ragweed biotype with this Common Ragweed biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on Group B/2 resistant Common Ragweed have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

The mechanism of resistance for this biotype is either unknown or has not been entered in the database. If you know anything about the mechanism of resistance for this biotype then please update the database.

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of Group B/2 resistant Common Ragweed from Wisconsin please update the database.

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CONTRIBUTING WEED SCIENTISTS

THOMAS BUTTS

Assistant Professor, Extension Weed Scientist University of Arkansas System Division of Agriculture Crop, Soil and Environmental Sciences 2001 Hwy 70 E Lonoke, 72086, Arkansas United States Email Thomas Butts Web : Web Site Link

VINCE DAVIS (MOVED)

No Longer at University of Wisconsin University Of Wisconsin-Madison Department Of Agronomy 1575 Linden Drive Madison, 53706, Wisconsin United States Email Vince Davis (moved) Web : Web Site Link

DAVID STOLTENBERG

Professor University of Wisconsin-Madison Agronomy 1575 Linden Dr Madison, 53706-1514, Wisconsin United States Email David Stoltenberg Web : Web Site Link

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Wisconsin have been instrumental in providing you this information. Particular thanks is given to Thomas Butts, Vince Davis (moved), and David Stoltenberg for providing detailed information.

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Herbicide Resistant Common Ragweed Globally
(Ambrosia artemisiifolia)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Canada (Ontario)

1976

Corn (maize), and Cropland

atrazine

Photosystem II inhibitors (C1/5)

Canada (Quebec)

1999

Carrots

linuron

PSII inhibitor (Ureas and amides) (C2/7)

Canada (Quebec)

1999

Carrots

linuron, and metribuzin

Multiple Resistance: 2 Sites of Action
Photosystem II inhibitors (C1/5)
PSII inhibitor (Ureas and amides) (C2/7)

Canada (Ontario)

2000

Soybean

chlorimuron-ethyl, cloransulam-methyl, and imazethapyr

ALS inhibitors (B/2)

Canada (Quebec)

2007

Soybean

cloransulam-methyl, and imazethapyr

ALS inhibitors (B/2)

Canada (Ontario)

2012

Soybean

chlorimuron-ethyl, cloransulam-methyl, glyphosate, and imazamethabenz-methyl

Multiple Resistance: 2 Sites of Action
ALS inhibitors (B/2)
EPSP synthase inhibitors (G/9)

United States (Michigan)

1990

Corn (maize), and Nurseries

atrazine

Photosystem II inhibitors (C1/5)

United States (New York)

1993

Corn (maize)

atrazine, cyanazine, and simazine

Photosystem II inhibitors (C1/5)

United States (Indiana)

1998

Soybean

cloransulam-methyl, and imazethapyr

ALS inhibitors (B/2)

United States (Illinois)

1998

Soybean

cloransulam-methyl, and imazethapyr

ALS inhibitors (B/2)

United States (Michigan)

1998

Corn (maize), Nurseries, and Soybean

cloransulam-methyl, imazamox, and imazethapyr

ALS inhibitors (B/2)

United States (Minnesota)

1998

Soybean

cloransulam-methyl, imazethapyr, and primisulfuron-methyl

ALS inhibitors (B/2)

United States (Ohio)

1998

Soybean

chlorimuron-ethyl, cloransulam-methyl, halosulfuron-methyl, imazamox, imazaquin, primisulfuron-methyl, and prosulfuron

ALS inhibitors (B/2)

United States (Missouri)

2004

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Arkansas)

2004

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Delaware)

2005

Soybean

acifluorfen-sodium, carfentrazone-ethyl, chlorimuron-ethyl, cloransulam-methyl, flumiclorac-pentyl, flumioxazin, fomesafen, halosulfuron-methyl, imazamox, imazapyr, imazaquin, imazethapyr, iodosulfuron-methyl-sodium, lactofen, metsulfuron-methyl, oxyfluorfen, primisulfuron-methyl, pyraflufen-ethyl, pyrithiobac-sodium, sulfentrazone, and trifloxysulfuron-sodium

Multiple Resistance: 2 Sites of Action
ALS inhibitors (B/2)
PPO inhibitors (E/14)

United States (Ohio)

2006

Soybean

chlorimuron-ethyl, cloransulam-methyl, and glyphosate

Multiple Resistance: 2 Sites of Action
ALS inhibitors (B/2)
EPSP synthase inhibitors (G/9)

United States (Ohio)

2006

Soybean

chlorimuron-ethyl, cloransulam-methyl, fomesafen, and lactofen

Multiple Resistance: 2 Sites of Action
ALS inhibitors (B/2)
PPO inhibitors (E/14)

United States (North Carolina)

2006

Cotton

glyphosate

EPSP synthase inhibitors (G/9)

United States (North Carolina)

2006

Peanut (groundnut)

diclosulam

ALS inhibitors (B/2)

United States (Kentucky)

2006

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Kansas)

2007

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (North Dakota)

2007

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Indiana)

2007

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (South Dakota)

2007

Corn (maize), and Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Minnesota)

2008

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Pennsylvania)

2008

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Minnesota)

2010

Soybean

cloransulam-methyl, glyphosate, and imazapyr

Multiple Resistance: 2 Sites of Action
ALS inhibitors (B/2)
EPSP synthase inhibitors (G/9)

United States (Alabama)

2013

Cotton

glyphosate

EPSP synthase inhibitors (G/9)

United States (New Jersey)

2013

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Nebraska)

2013

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (Wisconsin)

2013

Soybean

cloransulam-methyl

ALS inhibitors (B/2)

United States (Mississippi)

2014

Soybean

glyphosate

EPSP synthase inhibitors (G/9)

United States (North Carolina)

2015

Corn (maize), and Soybean

acifluorfen-sodium, cloransulam-methyl, fomesafen, glyphosate, lactofen, and nicosulfuron

Multiple Resistance: 3 Sites of Action
ALS inhibitors (B/2)
PPO inhibitors (E/14)
EPSP synthase inhibitors (G/9)

United States (Michigan)

2016

Soybean

cloransulam-methyl, and fomesafen

Multiple Resistance: 2 Sites of Action
ALS inhibitors (B/2)
PPO inhibitors (E/14)

United States (Maryland)

2016

Soybean

cloransulam-methyl, fomesafen, and glyphosate

Multiple Resistance: 3 Sites of Action
ALS inhibitors (B/2)
PPO inhibitors (E/14)
EPSP synthase inhibitors (G/9)

United States (New Jersey)

2016

Soybean

cloransulam-methyl, fomesafen, and glyphosate

Multiple Resistance: 3 Sites of Action
ALS inhibitors (B/2)
PPO inhibitors (E/14)
EPSP synthase inhibitors (G/9)

United States (Wisconsin)

2017

Corn (maize), and Soybean

glyphosate

EPSP synthase inhibitors (G/9)

Literature about Similar Cases

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Danielis, R.. 2013. Weeding trials in soybeans in 2013: control of Ambrosia artemisiifolia. Notiziario ERSA : 20 - 22.

This paper presents the results of two experiments conducted in 2013 using pre-emergence and post-emergence herbicides to control Ambrosia artemisiifolia in soyabean fields in Friuli Venezia Giulia, Italy. Among the pre-emergence herbicides, metribuzin was the most effective in controlling Ambrosia artemisiifolia. Among the post-emergency treatments, thifensulfuron-methyl was the most active against the weed. Some suggestions are given for effective control of Ambrosia artemisiifolia, which include crop rotation to avoid the development of herbicide-resistant grasses..

Dinelli, G. ; Marotti, I. ; Catizone, P. ; Bosi, S. ; Tanveer, A. ; Abbas, R. N. ; Pavlovic, D.. 2013. Germination ecology of Ambrosia artemisiifolia L. and Ambrosia trifida L. biotypes suspected of glyphosate resistance. Central European Journal of Biology 8 : 286 - 296.

The germination ecology of Ambrosia artemisiifolia and A. trifida glyphosate susceptible biotypes sampled in marginal areas, was compared with that of the same species but different biotypes suspected of glyphosate resistance, common and giant ragweed, respectively. The suspected resistant biotypes were sampled in Roundup Ready® soybean fields. Within each weed species, the seeds of the biotype sampled in marginal area were significantly bigger and heavier than those of the biotype sampled in the soybean fields. A. artemisiifolia biotypes exhibited a similar dormancy and germination, while differences between A. trifida biotypes were observed. A. artemisiifolia biotypes showed similar threshold temperature for germination, whereas, the threshold temperature of the susceptible A. trifida biotype was half as compared to that of the resistant A. trifida biotype. No significant differences in emergence as a function of sowing depth were observed between susceptible A. artemisiifolia and suspected resistant A. trifida biotype, while at a six-cm seedling depth the emergence of the A. artemisiifolia susceptible biotype was 2.5 times higher than that of the A. trifida suspected resistant biotype. This study identified important differences in seed germination between herbicide resistant and susceptible biotypes and relates this information to the ecology of species adapted to Roundup Ready® fields. Information obtained in this study supports sustainable management strategies, with continued use of glyphosate as a possibility..

Rousonelos, S. L. ; Lee, R. M. ; Moreira, M. S. ; VanGessel, M. J. ; Tranel, P. J.. 2012. Characterization of a common ragweed (Ambrosia artemisiifolia) population resistant to ALS- and PPO-inhibiting herbicides. Weed Science 60 : 335 - 344.

A population of common ragweed from Delaware was not controlled in the field by herbicides that inhibit acetolactate synthase (ALS) or protoporphyrinogen oxidase (PPO). Research was conducted to ascertain if this population was resistant to these herbicidal modes of action and, if so, to determine the resistance mechanism(s). Resistance was confirmed by dose-response studies on greenhouse-grown plants with multiple ALS- and PPO-inhibiting herbicides. DNA sequence data revealed that resistance to ALS-inhibiting herbicides was due to the previously reported W574L ALS mutation. To assist in determining the mechanism of resistance to PPO-inhibiting herbicides, an F₂ population was derived from a cross between the resistant biotype (Del-R) and a sensitive biotype (DV1-S). This population segregated in the ratio of three resistant one sensitive when treated with fomesafen, indicating that resistance to PPO-inhibiting herbicides was conferred by a single, (incompletely) dominant, nuclear gene. Sequences of the target-site genes, PPX1 and PPX2, for PPO-inhibiting herbicides were obtained through the screening of a common ragweed cDNA library and subsequent cDNA extension (5′-RACE). Molecular marker analysis with the F₂ population revealed that the PPX2 gene cosegregated with resistance to PPO-inhibiting herbicides. A mutation substituting an arginine codon for a leucine codon at a conserved location (R98L) of the PPX2 gene was suspected of being responsible for resistance. By using a transgenic Escherichia coli system, it was demonstrated that the R98L mutation was sufficient to confer resistance to PPO-inhibiting herbicides. The level of resistance to acifluorfen conferred by the R98L mutation in the E. coli system was about 31-fold, similar to the level of resistance seen in the whole-plant dose-response study. Last, a DNA-based assay was developed to identify the presence or absence of the common ragweed PPX2 R98L mutation. The R98L PPX2 mutation is the second mechanism identified for evolved resistance to PPO-inhibiting herbicides..

Chandi, A. ; Jordan, D. L. ; York, A. C. ; Lassiter, B. R.. 2012. Confirmation and management of common ragweed (Ambrosia artemisiifolia) resistant to diclosulam. Weed Technology 26 : 29 - 36.

Selection for biotypes of common ragweed expressing resistance to acetolactate synthase (ALS)-inhibiting herbicides has increased in North Carolina and surrounding states. Research was conducted in North Carolina to confirm common ragweed resistance to diclosulam and to compare herbicide programs designed to control ALS-resistant common ragweed in corn, cotton, peanut, and soybean. In greenhouse experiments, 50% inhibition values following POST application of diclosulam for mortality of plants, visual estimates for percentage of control, and percentage of reduction in plant fresh weight were 557- to 653-fold higher for the suspected ALS-resistant biotype compared with a suspected ALS-susceptible biotype. Herbicides with different modes of action, including atrazine, dicamba, and glyphosate in corn; fomesafen, glyphosate, MSMA, and prometryn in cotton; bentazon, flumioxazin, and lactofen in peanut; and flumioxazin, glyphosate, and lactofen in soybean controlled common ragweed more effectively than programs relying on cloransulam-methyl (soybean), diclosulam (peanut), thifensulfuron (corn), and trifloxysulfuron (cotton), which typically control nonresistant common ragweed populations. Applying tank-mix or sequential applications of herbicides with different modes of action was effective in controlling ALS-resistant common ragweed in all crops..

Mátyás, K. K. ; Taller, J. ; Cseh, A. ; Cernák, P. P. I.. 2011. Development of a simple PCR-based assay for the identification of triazine resistance in the noxious plant common ragweed (Ambrosia artemisiifolia) and its applicability in higher plants. Biotechnology Letters 33 : 2509 - 2515.

Bidirectional allele-specific PCR (Bi-PASA) was used to detect a point mutation causing triazine resistance in common ragweed (Ambrosia artemisiifolia). The external primers amplified a 278 bp standard DNA fragment in all genotypes. In the susceptible S264S genotypes, a 208 bp fragment was expected while in resistant S264G common ragweed genotypes a 109 bp band was expected. In resistant plants, both the wild and mutant type fragments were detected, indicating that the original triazine sensitive cpDNA is maintained in a heteroplasmic state in the resistant S264G genotypes. Additionally, in silico analysis confirmed the potential applicability of our diagnostic assay for other plant species. In 24 out of 74 taxa (32%), the assay could be used without any change, while in the others some of the primers should be redesigned before use..

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